Hemodynamic consequences of left ventricular hypertrophy in spontaneously hypertensive rats.

Compared with hearts from normotensive rats isolated, perfused hearts from spontaneously hypertensive rats exhibit a rightward shift of the Frank-Starling curve in the lower range of filling pressures, that is, up to 10 mm Hg. The extent of this shift is proportional to the degree of left ventricular hypertrophy. This is suggested to be a consequence of an altered relation between end-diastolic pressure and end-diastolic tension of the progressively more thick-walled left ventricle. Furthermore, the cardiac function curves revealed that maximal cardiac performance is apparently better in spontaneously hypertensive rats than in normotensive rats at increased levels of afterload. Therefore, left ventricular hypertrophy in established hypertension seems to contribute to adjustment of cardiac performance to the enhanced pressure work in hypertension; however, this occurs at the expense of a rightward shift of the Frank-Starling curve. In spontaneously hypertensive rats studied in vitro, coronary vascular resistance per unit weight of tissue was increased at maximal dilation, as was maximal pressor response. This may reflect the same type of structural vascular adaptation that occurs in most systemic vascular beds in hypertension and that contributes to maintenance of increased vascular reactivity and flow resistance in both hypertensive patients and spontaneously hypertensive rats. Apparently as a consequence of this adaptation, splanchnic nerve stimulation at an increasing rate caused exaggerated increases in resistance in anesthetized hypertensive rats by comparison with findings in normotensive rats. However, the effect of capacitance vessel constriction on stroke volume caused by splanchnic nerve stimulation was less pronounced in hypertensive rats. This relative “hyporeactivity” of the capacitance vessels also suggests an altered relation between cardiac filling pressure and stroke volume of the hypertrophied left ventricle in the spontaneously hypertensive rat.